A new animal model of systemic sclerosis

为了评价抗DNA拓扑异构酶I抗体的作用，观察了Topo I联合弗氏完全佐剂(CFA)和弗氏不完全佐剂(IFA)治疗小鼠的组织纤维化和细胞因子的产生。与Topo I和IFA治疗相比，Topo I和CFA治疗可诱导皮肤和肺纤维化，并增加IL-6和IL-17的产生。Topo I和CFA组小鼠的抗Topo I抗体水平高于Topo I组和IFA组。此外，Topo I和CFA组小鼠支气管肺泡灌洗液中Th2和Th17细胞的频率增加，而Topo I和IFA组的Th1和Treg细胞频率增加。此外，IL-6的表达缺失改善了皮肤和肺纤维化，降低了Th2和Th17细胞频率。本研究表明，Topo I和CFA联合治疗可诱导SSC样组织纤维化和自身免疫。

To assess the contribution of anti-DNA topoisomerase I(anti-topo I)antibody, tissue fibrosis and cytokine production were examined in mice treated with topo I and either Freund's complete adjuvant (CFA) or Freund's incomplete adjuvant(IFA).Treatment with topo I and CFA,in contrast to treatment with topo I and IFA,induced skin and lung fibrosis with increased interleukin (IL)-6 and IL-17 production. Anti-topo I antibody levels were greater in mice treated with topo I and CFA than with topo I and IFA.Furthermore,treatment with topo I and CFA increased Th2 and Th17 cell frequencies in bronchoalveolar lavage fluid,whereas treatment with topo I and IFA increased Th1 and Treg cell frequencies.Moreover,loss of IL-6 expression ameliorated skin and lung fibrosis and decreased Th2 and Th17 cell frequencies. This study shows that treatment with topo I and CFA induces SSc-like tissue fibrosis and autoimmunity.